Blood adipocytokine concentration in patients with peripheral artery disease.

BACKGROUND: Inflammatory responses mediated by adipocytokines may affect both atherosclerosis development and progression, as well as the risk of in-stent restenosis. The aim of this study was to determine the relationships between blood leptin, adiponectin and tumor necrosis factor-α (TNF-α) concentrations and the 1-year outcome of superficial femoral artery (SFA) stenting. METHODS: Blood concentrations of leptin, adiponectin and TNF-α were determined in 70 patients undergoing SFA stenting due to intermittent claudication and in 40 patients undergoing carotid artery stenting (CAS). All subjects were followed up for at least 1 year in relation to the occurrence of clinically driven target lesion revascularization (TLR) or a major adverse cardiovascular event (MACE). RESULTS: Patients undergoing SFA stenting and CAS had similar blood adipocytokine concentrations. Patients with diabetes mellitus presented a higher leptin concentration, lower adiponectin-to-leptin ratio, and lower blood adiponectin concentration indexed to fat mass (FM) and to visceral adiposity score (VAS). In Kaplan-Meier analysis, blood concentration of TNF-α indexed to FM and to VAS was higher in patients who underwent TLR and MACE. However, in multifactorial analysis, the severity of atherosclerosis lesions in the femoropopliteal vascular region, estimated in relation to TASC-II classification, was the only predictor of TLR. CONCLUSIONS: Circulating adipocytokines did not distinguish patients with different clinical manifestations of atherosclerosis. Higher ratios of TNF-α -to-FM and to VAS before SFA stenting were related to TLR and MACE occurrence. Dysregulation in adipocytokine secretion may be a potential mediator of a proatherogenic action of diabetes mellitus in patients with peripheral artery disease.

Overweight and obesity versus concentrations of VEGF-A, sVEGFR-1, and sVEGFR-2 in plasma of patients with lower limb chronic ischemia.

OBJECTIVE: Being overweight or obese comprises a significant risk factor for atherosclerosis. Fat tissue also generates factors stimulating angiogenesis, the process by which new blood vessels form. The purpose of this paper is to assess concentrations of the vascular endothelial growth factor A (VEGF-A) and its soluble type-1 and type-2 receptors (sVEGFR-1 and sVEGFR-2) in plasma of patients with peripheral arterial disease (PAD) depending on the level of nutrition according to body mass index (BMI). METHODS: The study group included patients suffering from symptomatic PAD (n=46) in Fontaine classes IIa-IV without any history of neoplastic disease and who have a normal BMI (n=15), are overweight (n=21) or are obese (n=10). The control group (n=30) consisted of healthy non-smoking volunteers who were neither overweight nor obese. Venous blood plasma samples were collected from both groups at rest in the morning to determine plasma concentrations of VEGF-A, sVEGFR-1, and sVEGFR-2 using the enzyme-linked immunosorbent assay (ELISA) method. RESULTS: The group of patients with PAD co-existent with being overweight or obese tended to have higher mean concentration levels of VEGF-A and sVEGFR-2 when compared with patients suffering from PAD with normal BMI. A statistically significant positive correlation was obtained between BMI and average plasma concentrations of sVEGFR-2 (R=0.37, P=0.0103). However, no significant correlation was noticed between BMI and VEGF-A or sVEGFR-1 concentrations. CONCLUSIONS: A positive correlation determined between the level of antiangiogenic factor and BMI value may be indicative of the linearly growing prevalence of some antiangiogenic factors in patients with metabolic disorders, which may be one of numerous factors contributing to incomplete efficiency of collateral circulation development in patients with PAD.

Impact of type 2 diabetes on the plasma levels of vascular endothelial growth factor and its soluble receptors type 1 and type 2 in patients with peripheral arterial disease.

OBJECTIVE: Type 2 diabetes coexistent with lower extremity artery disease (peripheral arterial disease (PAD)) can be observed in numerous patients. The mechanism compensating for ischemia and contributing to healing is angiogenesis-the process of forming new blood vessels. The purpose of this study was to assess the likely impact of type 2 diabetes on the plasma levels of proangiogenic factor (vascular endothelial growth factor A (VEGF-A)) and angiogenesis inhibitors (soluble VEGF receptors type 1 and type 2 (sVEGFR-1 and sVEGFR-2)) in patients with PAD. METHODS: Among 46 patients with PAD under pharmacological therapy (non-invasive), we identified, based on medical history, a subgroup with coexistent type 2 diabetes (PAD-DM2+, n=15) and without diabetes (PAD-DM2-, n=31). The control group consisted of 30 healthy subjects. Plasma levels of VEGF-A, sVEGFR-1, and sVEGFR-2 were measured using the enzyme-linked immunosorbent assay (ELISA) method. RESULTS: The subgroups of PAD-DM2+ and PAD-DM2- revealed significantly higher concentrations of VEGF-A (P=0.000 007 and P=0.000 000 1, respectively) and significantly lower sVEGFR-2 levels (P=0.02 and P=0.000 01, respectively), when compared with the control group. Patients with PAD and coexistent diabetes tended to have a lower level of VEGF-A and higher levels of sVEGFR-1 and sVEGFR-2 comparable with non-diabetic patients. CONCLUSIONS: The coexistence of type 2 diabetes and PAD is demonstrated by a tendency to a lower plasma level of proangiogenic factor (VEGF-A) and higher levels of angiogenesis inhibitors (sVEGFR-1 and sVEGFR-2) at the same time. Regardless of the coexistence of type 2 diabetes, hypoxia appears to be a crucial factor stimulating the processes of angiogenesis in PAD patients comparable with healthy individuals, whereas hyperglycemia may have a negative impact on angiogenesis in lower limbs.

[Angina pectoris due to coronary-subclavian steal syndrome caused by the LIMA graft in the patient after CABG with the use of the right and left mammary artery]. / Dlawica piersiowa niestabilna spowodowana zespolem podkradania wiencowo-podobojczykowego przez LIMA z jednoczesnym krytycznym zwezeniem RIMA u pacjenta po CABG z uzyciem dwóch tetnic piersiowych wewnetrznych.

We present a case of a patient with unstable angina pectoris two years after coronary artery by-pass graft surgery with the use of the right and left mammary artery. The symptoms were caused by the critical RIMA stenosis and coronary-subclavian steal syndrome through the LIMA graft. Unsuccessful attempt of percutaneous angioplasty of the closed left subclavian artery was made. The angioplasty of the proximal part of the RIMA with the implantation of a drug eluting stent followed by the angioplasty of both left circumflex artery and obtuse marginal artery with the implantation of bare metal stents was performed. These procedures resulted in disappearance of anginal symptoms. Neurological examination did not reveal any signs of vertebrobasilar steal.

The effect of eight weeks of rabeprazole therapy on nitric oxide plasma level and esophageal pH and motility and motility nitric oxide plasma level in patients with erosive esophagitis.

BACKGROUND: Esophageal clearance, an important pathogenetic factor in gastroesophageal reflux disease, depends mainly on motility. Motility disturbances can be secondary to gastric output reflux. Nitric oxide influences esophageal motility. The aim of this study was to determine the effect of eight weeks of gastric acid secretion suppression with rabeprazole (20 mg/day) on esophageal motility. MATERIAL/METHODS: 20 patients with erosive esophagitis were studied. At study start and two weeks after the end of therapy, we recorded the results of interview, endoscopy, gastric and esophageal mucosa biopsy, 24-h esophageal pH-metry and manometry, and NO metabolites plasma concentration, determined spectrophotometrically (OXIS). RESULTS: All patients reported improvement and remained free of symptoms two weeks later. In 60% of cases, improvement of esophageal mucosa appearance was observed in endoscopic and histological examination. In follow-up we found a significantly smaller number of acid gastrooesophageal refluxes (p<0.05), reduced DeMeester score for pH range >7 (p<0.05), and greater % of time within the esophageal pH range 6-7 (p<0.05). Other esophageal pH-metry and 24-h manometry parameters did not change significantly. NO metabolites plasma concentration increased significantly (p=0.039). CONCLUSIONS: Clinical improvement after eight weeks of therapy with rabeprazole was connected with endoscopic changes only in 60% of our patients. Rabeprazole therapy did not influence esophageal motility, despite increased plasma levels of NO metabolites. Patients with erosive esophagitis need maintenance therapy, since as soon as two weeks after the end of treatment the % of monitoring time with esophageal pH<4 was similar to study start.